[acetyl-1-14C]-coenzyme A

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 脂肪酰基
• 英文名称: [acetyl-1-14C]-coenzyme A
• 英文别名: [1-¹⁴C]acetyl-CoA；[acetyl-1-14C]-acetyl-coenzyme A；[14C]acetylCoA；S-[2-[3-[[(2R)-4-[[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-4-hydroxy-3-phosphonooxyoxolan-2-yl]methoxy-hydroxyphosphoryl]oxy-hydroxyphosphoryl]oxy-2-hydroxy-3,3-dimethylbutanoyl]amino]propanoylamino]ethyl] (114C)ethanethioate
• 化学式: C₂₃H₃₈N₇O₁₇P₃S
• 分子量: 811.568
• InChiKey: ZSLZBFCDCINBPY-YHBLMJDYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -5.6
• 重原子数：
  51
• 可旋转键数：
  20
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.65
• 拓扑面积：
  389
• 氢给体数：
  9
• 氢受体数：
  22

反应信息

• 作为反应物：
  描述：

  [acetyl-1-14C]-coenzyme A 、 芳樟醇 在 sodium metabisulfite 、 Origanum dayi alcohol acetyl transferase 作用下， 以 甘油 为溶剂， 反应 0.5h， 生成
  参考文献：
  名称：

  Enantioselective monoterpene alcohol acetylation in Origanum, Mentha and Salvia species

  摘要：

  Selected plants within the Origanum, Mentha and Salvia genera, that contain significant amounts of chiral volatile alcohols and their related acetates, exhibit remarkable enantioselectivity of alcohol acetyl transferase (AAT) activity and particularly can discriminate between linalool enantiomers. Origanum dayi AAT produced almost enantiomerically pure (R)-linalyl acetate by enzymatic acetylation of racemic linalool, whereas the closely related O. majorana AAT produced a mixture of (R)- and (S)-linalyl acetate with a ratio of 6:4. V-max of O. dayi acetylation activity was 30-fold higher for (R)-linalool, whereas in O. majorana no such differences were found. (C) 2008 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.phytochem.2008.07.018

文献信息

• Inhibitors of sorotonin N-acetyltransferase
  申请人：The Rockefeller University

  公开号：US05990094A1

  公开（公告）日：1999-11-23

  This invention is directed to a compound having the formula I. ##STR1## This invention is directed to a pharmaceutical composition comprising a compound which inhibits serotonin N-acetyltransferase having the formula I and a pharmaceutical acceptable carrier. The present invention relates to novel compounds and analogs which inhibit the serotonin N-acetyltransferase enzyme, and to processes for their preparation.

  本发明涉及具有I式的化合物。##STR1## 本发明涉及一种制药组合物，包括具有I式的抑制血清素N-乙酰转移酶的化合物和一种制药可接受的载体。本发明涉及抑制血清素N-乙酰转移酶酶的新型化合物和类似物，以及它们的制备方法。
• Assessing the health risks following environmental exposure to hexachlorobutadiene
  作者：Trevor Green、Robert Lee、David Farrar、James Hill

  DOI：10.1016/s0378-4274(02)00372-7

  日期：2003.2

  Hexachloro-1,3-butadiene (HCBD) has been reported to be toxic to the rat kidney in a 2 year study at doses higher than 0.2 mg/kg/day. The toxicity is known to be a consequence of the metabolism of HCBD by glutathione conjugation and the renal beta-lyase pathway. Neither toxicity data, nor data on the metabolism of HCBD, are available in humans. In the current work, the potential of HCBD to cause kidney damage in humans environmentally exposed to this chemical has been assessed quantitatively by comparing the key metabolic steps in rats and humans. To that end, the hepatic conjugation of HCBD with glutathione, the metabolism of the cysteine conjugate by renal beta-lyases and N-acetyltransferases, and the metabolism of the N-acetylcysteine conjugate by renal acylases has been compared in vitro in rat and human tissues. Rates for each metabolic step were lower in humans than in rats; 5-fold for glutathione conjugation, 3-fold for beta-lyase and 3.5-fold for N-acetyltransferase. Acylase activity could not be detected in human kidney cytosol. Use of these data in a physiologically based toxicokinetic model to quantify metabolism by the beta-lyase pathway demonstrated that metabolism in humans was an order of magnitude lower than that in rats. At the no effect level for kidney toxicity in the rat the concentration of beta-lyase metabolites was calculated by the model to be 137.7 mg/l. In humans the same concentration would be achieved following exposure to 1.41 ppm HCBD. This is in contrast to the figure of 0.6 ppb which is obtained when it is assumed that the risk is associated with the internal dose of HCBD itself rather than beta-lyase metabolites. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.